IgE Immunology Flashcards
Type I hypersensitivity
Allergic responses mediated by IgE
Type II hypersensitivity
Antibody directed against tissue antigens- mediated by IgG
Type III hypersensitivity
Immune Complex mediated disease- mediated by antigen+IgG
Type IV hypersensitivity
delayed hypersensitivity mediated by T cells
Atopy
Atopy – genetic predisposition to develop IgE antibodies upon exposure to environmental allergens
• ALMOST ANY PROTEIN CAN INDUCE AN ALLERGIC RESPONSE IN AN ATOPIC INDIVIDUAL
Allergy
A disease induced by reaction to a usually innocuous antigen
IgE
standard Ig structure, heavily glycosylated and has binding sites for Fc(epsilon)R. Normally very low concentration in serum, usually cell bound found at host-environment interfaces. Binding sites for Fc(epsilon)R on mast cells and basophils
3 manifestations of allergic reactions
anaphylactic shock, allergic rhinitis, and chronic bronchial asthma
Both mast cells and basophils
Both express HIGH affinity FcεR
Both contain histamine, TNF-α and leukotrienes in cytoplasm
Degranulation releases the mediators
Mast cells
Mast cells - tissue bound, compartmentalized as mucosal or connetive tissue, contain potent vasoactive compounds and cytokines
Types of Mast cells
MC-tryptase (prominent within the mucosa of the respiratory and gastrointestinal tracts) and MC- tryptase and chymase (localized within connective tissue, such as the dermis, submucosa of the GI, heart, conjunctivae, and perivascular tissues)
common component of allergens
Chitin- a polysaccharide not found in mammals. This induces expression of chitinase- a possible inducer of allergenic antigen generation and release of vasoactive mediators
type of proteins that commonly become allergenic
Almost anything can be an allergen but there is a trend towards proteins with enzymatic activity or ones that induce it
Timing is important: decreased early exposure to infections in the genetically predisposed individual is associated with insufficient T regulator control of IgE (more later)
route - mucosal exposures predominate
First step of an allergic rxn
allergen taken up and presented by DCs, Th2 response activates (IL-4) B-cells which produce mostly IgE antibodies. IgE Abs bind mast cells and cause degranulation
Fc(epsilon)R
the only FcR that can be activated/bound by Ig not bound to antigen
Early response
WITHIN 15 MINUTES
PROSTAGLANDINS & LEUKOTRIENE RELEASE
DIRECT COMPLEMENT ACTIVATION
CANNOT HAPPEN IF NO PREVIOUS EXPOSURE
Late response
COMPLETELY DEPENDENT ON Th2 ACTIVATION
AND CYTOKINES IL3,4,5,13,AND 10
EOTAXIN
CHARACTERIZED BY EOSINOPHILS
clinical manifestations of an allergic response depend on
the location/site of reaction
Anaphylaxis
systemic, entry via stings, ingestion or inhalation(rare), typical allergens are insect venom, drugs, foods. Main symptoms are shock, hypotension, wheezing, urticaria and angioedema
eczema (atopic dermatitis), urticaria, angioedema
mostly skin, usually do to contact ingestion or inhalation(rare). Causes are uncertain, food, and drugs. Main symptoms are pruritic, vesicular, swollen lesions
Allergic rhinitis, conjunctivitis
mainly affects nose and eyes. due to contact with mucous membrane. Allergens include pollens, dust mines, animal dander and molds. Causes runny nose, redness and itchy eyes.
Asthma
affects the lungs, caused by inhalation of pollens, dust mites, animal dander, and molds. Causes wheezing, dyspnea, tachypnea.
Allergic gastroenteropathy
affects the GI tract due to ingestion of various foods leads to pain, bloating, vomiting and diarrhea.
Hygiene hypothesis
Decreased childhood infection and later exposure
Early exposure to infections less allergy
Large families, rural residence and daycare associated with less allergy
Lack of early exposure associated with deficiency of Tregs that control IgE synethesis
